Transcriptome Characterization of Short Distance Transport Stress in Beef Cattle Blood

The transportation is a crucial phase in beef cattle industry, and the annual losses caused by beef cattle transport stress are substantial. Several studies have described the effect of long distance transportation stress on animal health, such as disorder in nervous, endocrine, immune, and metabolic system. However, molecular mechanisms underlying short distance transportation stress is still poorly understood. Present study aims to investigate the effect of short distance transportation by measuring the hematological indices and transcriptomic analysis. In this study, a total 10 Qinchuan cattle were used to compare the molecular characteristics of blood before and after transportation. We have found that a stress-related marker “white blood cell count (WBC)” increased significantly after transportation. The decrease in triglyceride (TG), cholestenone (CHO), high-density lipoprotein (HDL), and low-density lipoprotein (LDL) showed that energy expenditure was increased after transportation, but not enough to activate fatty decomposition. Intriguingly, the decrease of malondialdehyde (MDA) showed that cattle were more resilience to oxidative stress. The RNA-seq showed that 1,092 differentially expressed genes (DEGs) were found (329 up-regulated and 763 down-regulated) between group before and group after. The GO and KEGG enrichment showed that the metabolic pathway and B cell function related pathways were enriched. Furthermore, median absolute deviation (MAD) top 5,000 genes were used to construct a co-expression network by weighted correlation network analysis (WGCNA), and 11 independent modules were identified. Combing with protein-protein interaction (PPI) analysis, the verification of quantitative real-time PCR (qPCR) and the correlation of B cell function, structural maintenance of chromosomes 3 (SMC3), jun proto-oncogene (JUN), and C-X-C motif chemokine ligand 10 (CXCL10) were suggested as potential molecular markers in identification of short distance transportation. Collectively, the blood RNA-seq analysis and WGCNA indicated that the disorder of B cell differentiation, proliferation, survival, and apoptosis were the potential molecular mechanism in short distance transportation stress. In conclusion, our results provide the novel insight about potential biomarkers for short distance transportation stress, which may serve as for diagnosing and preventing this condition in beef industry.

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Small RNA-Seq Analysis Reveals miRNA Expression of Short Distance Transportation Stress in Beef Cattle Blood

Animals ◽

10.3390/ani11102850 ◽

2021 ◽

Vol 11 (10) ◽

pp. 2850

Author(s):

Mingli Wu ◽

Xiaoqin Tang ◽

Sayed Haidar Abbas Raza ◽

Haidong Zhao ◽

Qi Li ◽

...

Keyword(s):

Beef Cattle ◽

Short Distance ◽

Economic Losses ◽

Molecular Characteristics ◽

Hub Genes ◽

Long Distance ◽

Potential Health ◽

Before And After ◽

Cattle Blood ◽

Transportation Stress

Transportation is a crucial phase in the beef cattle industry, and the annual losses caused by beef cattle transport stress are substantial. Because of its huge economic losses, such as lower growth rate and even death, long-distance transportation stress has attracted more attention from beef production practitioners because of its huge economic losses. Compared with the long-distance transportation stress, the short-distance transportation stress was ignored for the reason of no obvious symptoms in cattle. Our previous study showed that the disorder of B cell function could be a potential health risk after short-distance transportation. However, the transcriptome details of the changes in the cattle blood after short-distance transportation and the molecular mechanisms for the regulation of the developmental process are not clearly known. In this study, a total of 10 Qinchuan cattle were used to compare the molecular characteristics of blood before and after short-distance transportation. The miRNA-seq showed that 114 differentially expressed miRNAs (DEMs) were found (40 upregulated and 74 downregulated) between two groups before and after transportation. Furthermore, more than 90% of the miRNAs with counts of more than 10 were used to construct a co-expression network by weighted correlation network analysis (WGCNA), and four independent modules were identified. According to their relationship with 30 hub genes, the turquoise module was the key module in this study. The regulator network of hub genes and miRNAs in the turquoise module was constructed by miRNAs targeting genes predicting, and the miRNAs had targeting sites within hub genes that could be identified as hub-miRNAs. Further, it showed that CD40 and ITPKB had the same targeting miRNAs (miR-339a/b), and the newly discovered hub miRNAs filled the gaps in our previous study about the relationship between hub genes in short-distance transportation stress and provided the potential utility for predicting and treatment of short-distance transportation stress in beef cattle.

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B cell-specific GPR55 deficiency promotes atherosclerosis

European Heart Journal ◽

10.1093/ehjci/ehaa946.3785 ◽

2020 ◽

Vol 41 (Supplement_2) ◽

Author(s):

R Guillamat-Prats ◽

D Hering ◽

M Rami ◽

C Haerdtner ◽

L Bindila ◽

...

Keyword(s):

Body Weight ◽

B Cells ◽

B Cell ◽

Mrna Expression ◽

Cell Function ◽

Metabolic Effects ◽

Atherosclerotic Plaques ◽

Funding Source ◽

Sequencing Analysis ◽

B Cell Function

Abstract Background Atherosclerosis is accompanied by an imbalance between resolving and pro-inflammatory lipid mediators. Targeting lipid signaling pathways might offer a new anti-inflammatory therapy for improving the clinical outcome in cardiovascular disease patients. We considered lysophosphatidylinositol (LPI) and its receptor G protein-coupled receptor (GPR)55 as a potential modulator of atherosclerosis. Its role in regulating atherosclerosis and B cell function is unknown. Hypothesis We assessed the hypothesis that GPR55 signaling causally affects atherosclerosis and whether it has a specific role in regulating B cell function in this disease. Methods Atherosclerotic plaques were compared between apolipoprotein E deficient (ApoE−/−) and ApoE−/−Gpr55−/− mice after 4 to 16 weeks Western Diet (WD; 0.15% cholesterol; n=12–15 per group). To specifically test the role of B cell GPR55 in atherosclerosis, we generated mixed chimeras by lethally irradiating low density lipoprotein receptor deficient (Ldlr−/−) mice and reconstituting with a mixture of μMT and wildtype (control) or μMT and Gpr55−/− bone marrow cells. Circulating B cells were sorted and bulk RNA sequencing analysis was performed. We performed lipid and immunostainings of murine aortic root plaques, qPCR and ELISA of tissue lysates, as well as multiplex analysis of plasma immunoglobulins. Leukocyte plasma and tissue counts were determined by flow cytometry. Results GPR55 expression in mouse and human atherosclerotic plaques was detected by immunostaining. Furthermore, we confirmed murine Gpr55 mRNA expression on sorted circulating B220+B cells via qPCR, which was higher compared to CD3+ T cells, while CD11+ myeloid cells as well as NK cells had only low Gpr55 mRNA levels. ApoE−/−Gpr55−/− mice had significantly larger plaques after 4&16 weeks WD compared to ApoE−/− controls, with more pronounced body weight increases and higher cholesterol levels at the 16 weeks WD time point. In addition, global Gpr55 deficiency resulted in enhanced aortic pro-inflammatory cytokine mRNA expression (IL-1β, IL-6, TNFα) and a massively upregulated IgG1 plasma levels and increased percentages of splenic germinal center and plasma cells. B-cell RNA-seq analysis showed 460 differential expressed regulated genes in the ApoE−/−Gpr55−/− compared to ApoE−/−. The main pathways affected were calcium ion transport, immunoglobulin production, negative regulation of phosphorylation, and cellular component morphogenesis, suggesting a dsysregulation of B cell function. B cell specific Gpr55 deficiency blunted the metabolic effects on body weight and cholesterol, but still translated in larger atherosclerotic plaques and elevated plasma IgG levels compared to the respective controls. Conclusion Both global and B cell-restricted Gpr55 deficiency promotes atherosclerosis and is associated with a more pro-inflammatory phenotype. Our findings suggest a novel role for GPR55 in regulating B cell development and function. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Deutsche Forschungsgemeinschaft (DFG)

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